Network Pharmacology Reveals Potential Targets and Mechanisms of Luteolin in Treating Small Vessel Vasculitis

Small vessel vasculitis encompasses various inflammations in blood vessels, with IgA vasculitis and antineutrophil cytoplasmic antibody-associated vasculitis being prominent types. Luteolin, a natural flavonoid found in diverse flora, displays notable anti-inflammatory properties, suggesting its therapeutic potential for inflammatory conditions. The study aims to scrutinize the plausible mechanism by which luteolin functions as a remedial entity for small vessel vasculitis. The study employed network pharmacology methods to investigate the potential therapeutic mechanisms of luteolin for small vessel vasculitis. Luteolin target genes were obtained from online databases, and disease-related target genes were collected from multiple sources. Our exploration into these foundational mechanisms involved protein-protein interaction networks, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes pathway analyses. The study identified 24 shared target genes between luteolin and small vessel vasculitis. The protein-protein interaction analysis highlighted key targets such as Protein kinase B alpha and Matrix metallopeptidase 9. Kyoto Encyclopedia of Genes and Genomes pathway enrichment unveiled participation in signaling pathways, including Tumor necrosis factor signaling, Vascular endothelial growth factor signaling, and Interleukin 17 signaling. Molecular docking analysis demonstrated stable binding between luteolin and Protein kinase B alpha, Matrix metallopeptidase 9, indicating potential therapeutic interactions. Luteolin may exhibits potential therapeutic effects for Small vessel vasculitis by interacting with Protein kinase B alpha and Matrix metallopeptidase 9 and involvement in Tumor necrosis factor signaling pathway, Vascular endothelial growth factor signaling pathway, Platelet activation, Interleukin 17 signaling pathway.